Considerable clinical and pathologic evidence suggests that subendocardial ischemia may occur in the pathologically hypertrophied left ventricle despite anatomically normal coronary arteries, and that this perfusion abnormality may contribute to the eventual development of cardiac failure in the chronically hypertrophied heart. Consequently, this study is designed to evaluate transmural myocardial perfusion at rest and during the stress of exercise and rapid cardiac pacing in the intact awake dog with stable left ventricular hypertrophy produced by chronic pressure or volume overload. Regional myocardial blood flow will be examined using radionuclide-labeled microspheres, while the metabolic significance of any apparent perfusion abnormalities will be evaluated by examining coronary sinus blood for evidence of myocardial production of lactate and adenosine derivatives. The pressure-flow characteristics of the coronary vascular system will be evaluated for evidence of functional abnormalities resulting from alteration of coronary vasomotor activity, or increased extravascular compressive forces acting on the intramural coronary vessels, which might compromise coronary blood flow. Studies of myocardial vascular density will determine whether insufficient growth of coronary vasculature relative to the degree of hypertrophy results in anatomically decreased vascularity in the hypertrophied heart. Dogs with overt cardiac failure secondary to chronic left ventricular hypertrophy will be studied to determine whether cardiac failure is accompanied by decreased coronary vasodilator reserve capacity and increased vulnerability to subendocardial underperfusion. The long-term goal of this research is to determine the extent and metabolic significance of perfusion abnormalities occurring in the pathologically hypertrophied heart, and to provide insight into the anatomic and functional alterations occurring during the hypertrophic process which may contribute to these abnormalities.